This investigation deals with the biochemical basis and mechanisms for maturation and stabilization of surfactant function in the developing rabbit fetus and newborn. Findings are being correlated with human clinical examples, especially the respiratory distress syndrome (RDS). Previous studies have established that lecithin alone is not an effective surfactant, but depends upon the acidic phospholipids, phosphatidylinositol (PI) and phosphatidylglycerol (PG) for stabilization. The synthesis and regulation of PI and PG have been studied and will continue to be studied, especially since final surfactant maturation is dependent upon production of PG. However, PG synthesis appears to be under control of blood levels of myo-inositol, which, thus effectively regulates surfactant maturation. Production of surfactant phospholipids by prematurely born infants appears to be accelerated by birth when studied by the lung profile so that infants of 800 gm to 2200 gm who have RDS make these compounds at the same rate and all have mature surfactant by about 72 hours. In very tiny infants (less than 1200 gm) many of the problems with RDS are attributable to another developmental problem, patent ductus arteriosus. Studies will be continued on these above problems, to further define them, as well as on surface characteristics of component phospholipids, the relationship of fetal membrane phospholipids and infection in premature labor, and development of a rabbit diabetes model with macrosomic and hyperinsulinemia.